PFDN6 / HKE2 Control Peptide antibody /CP
- Known as:
- PFDN6 / HKE2 Control Peptide (anti-) /CP
- Catalog number:
- 'AP12491CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- PFDN6 / HKE2 Control Peptide antibody
Related genes to: PFDN6 / HKE2 Control Peptide antibody /CP
- Gene:
- PFDN6 NIH gene
- Name:
- prefoldin subunit 6
- Previous symbol:
- HKE2
- Synonyms:
- KE-2, H2-KE2, PFD6
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-26
- Date modifiied:
- 2016-10-05
Related products to: PFDN6 / HKE2 Control Peptide antibody /CP
Related articles to: PFDN6 / HKE2 Control Peptide antibody /CP
- Tauopathies represent a major class of neurodegenerative disorders associated with intracellular aggregates of the microtubule-associated protein Tau. To identify molecular modulators of Tau toxicity, we used a genetic screen to identify protein chaperones whose RNAi-mediated knockdown could modulate hTau-induced eye-ommatidial degeneration in . This screen identified the Prefoldins Pfdn5 and Pfdn6 as strong modifiers of hTau cytotoxicity. Consistent with the known function of Pfdn as a cotranslational chaperone for tubulin, mutants showed substantially reduced levels of tubulin monomer. However, additional microtubule-related functions were indicated by the robust unexpected association of Pfdn5 with axonal microtubules in vivo, as well as binding with stabilized microtubules in biochemical assays. Loss of Pfdn5 resulted in neuromuscular junctions (NMJ) defects similar to those previously described in hTau-expressing flies: namely, increased supernumerary boutons and fewer microtubule loops within mature presynaptic boutons. Significantly, synaptic phenotypes caused by hTau overexpression were also strongly enhanced in a mutant background. Consistent with a role in modulating Tau toxicity, not only did loss of result in increased accumulations of Tau aggregates in hTau-expressing neurons, but also neuronal overexpression of Prefoldin strikingly ameliorated age-dependent neurodegeneration and memory deficits induced by pathological hTau. Together, these and other observations described herein: (a) provide new insight into Prefoldin-microtubule interactions; (b) point to essential post-translational roles for Pfdn5 in controlling Tau toxicity in vivo; and (c) demonstrate that Pfdn5 overexpression is sufficient to restrict Tau-induced neurodegeneration. - Source: PubMed
Publication date: 2026/01/14
Bisht AnjaliPippadpally SrikanthMajumder SnehasisGopi Athulya TDas AbhijitSahi ChandanRamaswami ManiKumar Vimlesh - The Plasmodium infection cycle in mosquitoes relies on numerous host factors in the vector midgut, which can be targeted with therapeutics. The mosquito prefoldin complex is needed to fold proteins and macromolecular complexes properly. Here we show that the conserved Anopheles mosquito prefoldin (PFDN)-chaperonin system is a potent transmission-blocking target for multiple Plasmodium species. Silencing any prefoldin subunit or its CCT/TRiC partner via RNA interference reduces Plasmodium falciparum oocyst loads in the mosquito midgut, as does co-feeding mosquitoes with PFDN6-specific antibody and gametocytes. Inhibition of the PFDN-CCT/TRiC chaperonin complex results in the loss of epithelial and extracellular matrix integrity, which triggers microorganism-mediated anti-Plasmodium immune priming and compromises the parasite's laminin-based immune evasion. Mouse malaria transmission-blocking vaccine and antibody co-feeding assays support its potential as a multispecies transmission-blocking target for P. falciparum and Plasmodium vivax. Further study is needed to determine the potential of this system as a transmission-blocking vaccine target. - Source: PubMed
Publication date: 2025/03/06
Dong YuemeiKang SeokyoungSandiford Simone LPike AndrewSimões Maria LUbalee RatawanKobylinski KevinDimopoulos George - Colorectal cancer (CRC) is a common cancer worldwide. Although there are several treatments for cancer, the therapeutic effect on CRC remains unsatisfactory, and it is imperative to identify new therapeutic targets. - Source: PubMed
Publication date: 2024/04/10
Xu FenghuaKong LingYangSun XiaoHui WenXiangJiang LanHan WenxinXiao ZhiFengLi NingChen DongFengZheng NanHan JingLiu Lei - The analysis of differentially expressed genes in muscle tissues of sheep at different ages is helpful to analyze the gene expression trends during muscle development. In this study, the longissimus dorsi muscle of pure breeding Hu sheep (H), Suffolk sheep and Hu sheep hybrid F1 generation (SH) and East Friesian and Hu sheep hybrid sheep (EHH) three strains of sheep born 2 days (B2) and 8 months (M8) was used as the research object, and transcriptome sequencing technology was used to identify the differentially expressed genes of sheep longissimus dorsi muscle in these two stages. Subsequently, GO and KEGG enrichment analysis were performed on the differential genes. Nine differentially expressed genes were randomly selected and their expression levels were verified by qRT-PCR. - Source: PubMed
Publication date: 2024/06/07
Wan SailuoLou MengyuZhang SihuanLi ShuangLing Yinghui - Gliomas are one of the most aggressive primary tumours, accounting for 81% of malignant brain tumours, and are associated with a significant mortality. Therefore, the elucidation of the molecular mechanism underlying glioma progression and identification of promising treatment targets are necessary. Here, the expression of prefoldin (PFDN) 6 in human glioma tissues and cell lines was evaluated using immunohistochemistry and quantitative polymerase chain reaction. Celigo and CCK-8 assays were performed for assessing cell viability. Flow cytometry was used to analyse apoptosis and cell cycle distribution. Wound-healing and transwell assays were performed to observe cell migration. Lastly, xenograft models were developed for the in vivo validation of the results, and a human phospho-kinase array was used to explore the downstream signalling pathways. PFDN6 was upregulated in gliomas, and PFDN6 overexpression was significantly correlated with a low survival rate, estimated glomerular filtration rate (EGFR) expression, and tumour grade and recurrence. Moreover, PFDN6 knockdown significantly attenuated cell proliferation and migration, induced apoptosis, and blocked cell cycle progression in the G2 phase, which was further confirmed in the in vivo experiments. Mechanistically, the effects of PFDN6 may be mediated via the AKT signalling pathway. In conclusion, we showed that PFDN6 promotes glioma development by activating AKT signalling and emphasised the potential of PFDN6 as a crucial target in glioma therapy. - Source: PubMed
Publication date: 2022/10/27
Jiang LiangleiLiu Jun